Clinical Reviews in Allergy & Immunology,
Journal Year:
2024,
Volume and Issue:
68(1)
Published: Dec. 27, 2024
Asthma
is
a
chronic
airway
inflammatory
disease
that
affects
millions
globally.
Although
glucocorticoids
are
mainstay
of
asthma
treatment,
subset
patients
show
resistance
to
these
therapies,
resulting
in
poor
control
and
increased
morbidity.
The
complex
mechanisms
underlying
steroid-resistant
(SRA)
involve
Th1
Th17
lymphocyte
activity,
neutrophil
recruitment,
NLRP3
inflammasome
activation.
Recent
studies
provided
evidence
innate
lymphoid
cells
type
3
(ILC3s)
might
be
potential
therapeutic
targets
for
non-eosinophilic
(NEA)
SRA.
Like
cells,
ILC3s
play
crucial
roles
immune
responses,
inflammation,
tissue
homeostasis,
contributing
severity
corticosteroid
NEA.
Biologics
targeting
ILC3-related
pathways
have
shown
promise
managing
Th2-low
asthma,
suggesting
new
avenues
SRA
treatment.
This
review
aims
explore
the
risk
factors
SRA,
discuss
challenges
consolidate
current
findings
on
elucidate
their
role
respiratory
conditions.
We
present
latest
involvement
human
diseases
development.
Furthermore,
we
emerging
biologics
NEA
highlights
challenges,
strategies,
addresses
significant
gap
research,
with
implications
improving
management
asthma.
Journal of Clinical Investigation,
Journal Year:
2024,
Volume and Issue:
134(13)
Published: June 30, 2024
Type
3
innate
lymphoid
cells
(ILC3s)
are
key
regulators
of
intestinal
homeostasis
and
epithelial
barrier
integrity.
In
this
issue
the
JCI,
Cao
colleagues
found
that
a
sensor
endoplasmic
reticulum
(ER)
stress,
inositol-requiring
kinase
1α/X-box-binding
protein
1
(IRE1α/XBP1)
pathway,
fine-tuned
functions
ILC3s.
Activation
IRE1α
XBP1
in
ILC3s
limited
inflammation
mice
correlated
with
efficacy
ustekinumab,
an
IL-12/IL-23
blocker,
patients
Crohn's
disease.
These
results
advance
our
understanding
use
ILCs
as
biomarkers
not
only
to
predict
disease
outcomes
but
also
indicate
response
biologicals
inflammatory
bowel
Mucosal Immunology,
Journal Year:
2024,
Volume and Issue:
17(6), P. 1212 - 1221
Published: Aug. 11, 2024
Group
3
innate
lymphoid
cells
(ILC3s)
are
abundant
in
the
developing
or
healthy
intestine
to
critically
support
tissue
homeostasis
response
microbial
colonization.
However,
intestinal
ILC3s
reduced
during
chronic
infections,
colorectal
cancer,
inflammatory
bowel
disease
(IBD),
and
mechanisms
driving
these
alterations
remain
poorly
understood.
Here
we
employed
RNA
sequencing
of
from
IBD
patients
observed
a
significant
upregulation
RIPK3,
central
regulator
necroptosis,
inflammation.
This
was
modeled
mice
where
found
that
express
with
conventional
(c)ILC3s
exhibiting
high
RIPK3
low
levels
pro-survival
genes
relative
inducer
(LTi)-like
ILC3s.
ILC3-specific
is
promoted
by
gut
microbiota,
further
upregulated
following
enteric
infection,
dependent
upon
IL-23R
STAT3
signaling.
lineage-specific
deletion
revealed
redundant
role
ILC3
survival,
due
blockade
RIPK3-mediated
necroptosis
caspase
8,
which
also
activated
infection.
In
contrast,
8
resulted
loss
cILC3s
all
subsets
increased
pathogen
burdens
function
required
catalytic
activity
induced
TNF
TL1A
dispensable
if
simultaneously
deleted.
Caspase
activation
cell
death
were
associated
Fas
on
ILC3s,
Fas-FasL
pathway
could
restrain
abundance
Collectively,
data
reveal
interpretation
key
cytokine
signals
controls
survival
challenge,
an
imbalance
pathways,
such
as
across
subsets,
provokes
depletion
tissue-protective
inflamed
intestine.
Clinical Reviews in Allergy & Immunology,
Journal Year:
2024,
Volume and Issue:
68(1)
Published: Dec. 27, 2024
Asthma
is
a
chronic
airway
inflammatory
disease
that
affects
millions
globally.
Although
glucocorticoids
are
mainstay
of
asthma
treatment,
subset
patients
show
resistance
to
these
therapies,
resulting
in
poor
control
and
increased
morbidity.
The
complex
mechanisms
underlying
steroid-resistant
(SRA)
involve
Th1
Th17
lymphocyte
activity,
neutrophil
recruitment,
NLRP3
inflammasome
activation.
Recent
studies
provided
evidence
innate
lymphoid
cells
type
3
(ILC3s)
might
be
potential
therapeutic
targets
for
non-eosinophilic
(NEA)
SRA.
Like
cells,
ILC3s
play
crucial
roles
immune
responses,
inflammation,
tissue
homeostasis,
contributing
severity
corticosteroid
NEA.
Biologics
targeting
ILC3-related
pathways
have
shown
promise
managing
Th2-low
asthma,
suggesting
new
avenues
SRA
treatment.
This
review
aims
explore
the
risk
factors
SRA,
discuss
challenges
consolidate
current
findings
on
elucidate
their
role
respiratory
conditions.
We
present
latest
involvement
human
diseases
development.
Furthermore,
we
emerging
biologics
NEA
highlights
challenges,
strategies,
addresses
significant
gap
research,
with
implications
improving
management
asthma.
